scholarly journals Cytosine methylation in the promoter region of genes involved in cellular oxidation equilibrium pathways affects rice heat tolerance

2020 ◽  
Author(s):  
Chao He ◽  
Hong-Yu Zhang ◽  
Yong-Xin Zhang ◽  
Pei Fu ◽  
Li-Li You ◽  
...  

Abstract Background High temperatures are detrimental to rice yield and quality, especially at night. Due to the predicted increases in global warming, it is imperative that crops are able to adapt to high night temperatures (HNTs) in the near future. DNA methylation is a potential mechanism for controlling gene activity and cellular phenotype under adversely environment without changing nucleotide sequence.Results Here, we reported that few CG and CHG contexts but CHH context in rice genome was strongly induced by HNT to occur cytosine methylation variation between two coisogenic rice strains with significant difference in heat tolerance. Methylation variations occurred mainly on successive cytosines in the promoter or downstream regions of transcription factors and transposon elements. In contrast to the heat-sensitive rice strain, two basal transcriptional factor TFIID subunit 11 and mediator of RNA polymerase II transcription subunit 31 were fully demethylated in the downstream 358-359 bp and 2-60 bp under HNT in the heat-tolerant strain, respectively. Various genes involved in ABA-related reactive oxygen species (ROS) equilibrium pathways, including the pentatricopeptide repeat domain gene PPR (LOC_Os07g28900) and the homeobox domain gene homeobox (LOC_Os01g19694), were induced by HNT to occur methylation variation on successive cytosines in the gene promoter regions of the heat-tolerant strain. Varidation among the typical heat-tolerant group and heat-sensitive group of rice germplasms, methylation rate of the cytosines in gene promoter region for gene PPR was higher and gene expression was suppressed in the heat-sensitive group, comparing to the heat-tolerant group.Conclusions The CHH context in rice genome was the main context type to occur cytosine methylation variation under HNT between the heat-sensitive and heat-tolerant rice strains. Methylation in the promoter regions of the genes related to abscisic acid-related oxidation and ROS scavenging contributes to rice heat tolerance. These findings provide bases to explain the molecular mechanisms behind rice heat tolerance.

2020 ◽  
Author(s):  
Chao He ◽  
Hong-Yu Zhang ◽  
Yong-Xin Zhang ◽  
Pei Fu ◽  
Li-Li You ◽  
...  

Abstract Background: High temperatures, particularly at night, decrease rice yield and quality. As high nighttime temperatures (HNTs) become increasingly frequent due to climate change, it is imperative to develop rice crops that tolerate HNTs. DNA methylation may represent a potential avenue for HNT-tolerant rice strain development, as this mechanism regulates gene activity and cellular phenotype in response to adverse environmental conditions without changing the nucleotide sequence.Results: After HNT exposure, the methylation patterns of cytosines in the CHH context differed noticeably between two coisogenic rice strains with significantly different levels in heat tolerance. Methylation differences between strains were primarily observed on successive cytosines in the promoter or downstream regions of transcription factors and transposon elements. In contrast to the heat-sensitive rice strain, the regions 358–359 bp and 2–60 bp downstream of two basal transcriptional factors (TFIID subunit 11 and mediator of RNA polymerase II transcription subunit 31, respectively) were fully demethylated in the heat-tolerant strain after HNT exposure. In the heat-tolerant strain, HNTs reversed the methylation patterns of successive cytosines in the promoter regions of various genes involved in abscisic acid (ABA)-related reactive oxygen species (ROS) equilibrium pathways, including the pentatricopeptide repeat domain gene PPR (LOC_Os07g28900) and the homeobox domain gene homeobox (LOC_Os01g19694). Indeed, PRR expression was inhibited in heat-sensitive rice strains, and the methylation rates of the cytosines in the promoter region of PRR were greater in heat-sensitive strains as compared to heat-tolerant strains.Conclusions: After HNT exposure, cytosines in the CHH context were more likely than cytosines in other contexts to be methylated differently between the heat-sensitive and heat-tolerant rice strains. Methylation in the promoter regions of the genes associated with ABA-related oxidation and ROS scavenging improved heat tolerance in rice. Our results help to clarify the molecular mechanisms underlying rice heat tolerance.


2005 ◽  
Vol 21 (1) ◽  
pp. 3-7 ◽  
Author(s):  
Xiao Feng Zhou ◽  
Jing Cui ◽  
Anita L. DeStefano ◽  
Irmarie Chazaro ◽  
Lindsay A. Farrer ◽  
...  

Genetic variations that predispose individuals to complex disorders, such as essential hypertension, may be found in gene coding regions, intronic regions or in gene promoter regions. Most studies have focused on gene variations that result in amino acid substitutions because they result in different isoforms of the protein, presumably resulting in differences in protein properties. Less attention has been placed on the role of intronic or promoter mutations. In this report, we examined two single nucleotide polymorphisms (SNPs) in the catalase (CAT) gene prompter region in a cohort of hypertensive Caucasians and African Americans with a Mass Spec based Homogenous MassEXTEND assay. We found an association when a specific combination of the two promoter SNPs was examined in Caucasians. No association was observed in African Americans. Our data suggest that genetic variations in the promoter region of catalase gene influence the susceptibility to essential hypertension. In addition, the genetic factors that contribute to hypertension maybe different between ethnic groups.


2018 ◽  
Vol 112 (1) ◽  
pp. 31
Author(s):  
Anja ČIBEJ ◽  
Simona SUŠNIK BAJEC

Salmonidae family combines freshwater and anadromous fish species. Duplicates of numerous genomic DNA loci are characteristic for this family, some as a consequence of tetraploidisation, and others as independent doubling of discrete DNA regions. In the genus <em>Salmo</em>, duplication of transferrin gene in Atlantic salmon, brown and marble trout has been demonstrated. The aim of the study was to characterize the promoter region of both genes (TF1 and TF2) in all three species and to determine the ratio of expression of TF1 and TF2 in Atlantic salmon. Applying qPCR we showed that TF2 is expressed in Atlantic salmon six times weaker than TF1. It has been previously shown that the difference in the expression of both genes in brown and marble trout is even higher. The nucleotide sequence was determined for promoter regions of both genes in all species. In promoter region, microsatellite was found, which differs in length as well within species as between TF1 and TF2 locus, and four SNPs that differentiate TF1 and TF2. For Atlantic salmon, longer sequence of promoter region was determined. In TF1 gene, promoter contains a minisatellite, comprised of 37 bp long motif with over 20 replicates, while in TF2 minisatellite is not present. Analyzing potential binding sites in promoter region, functional elements for regulation of transferrin gene expression were found.


Retrovirology ◽  
2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Peipei Yuan ◽  
Jun Yan ◽  
Shuang Wang ◽  
Yang Guo ◽  
Xueyan Xi ◽  
...  

Abstract Background Prototype foamy virus (PFV) is nonpathogenic complex retroviruses that express a transcriptional transactivator Tas, which is essential for the activity of viral long terminal repeat (LTR) promoter and internal promoter (IP). Tripartite motif-containing protein 28 (Trim28) is well known as a scaffold protein normally enriched in gene promoter region to repress transcription. We sought to determine if whether Trim28 could be enriched in PFV promoter region to participate the establishment of PFV latency infection. Results In this study, we show that Trim28 restricts Tas-dependent transactivation activity of PFV promoter and negatively regulates PFV replication. Trim28 was found to be enriched in LTR instead of IP promoter regions of PFV genome and contribute to the maintenance of histone H3K9me3 marks on the LTR promoter. Furthermore, Trim28 interacts with Tas and colocalizes with Tas in the nucleus. Besides, we found that Trim28, an E3 ubiquitin ligase, binds directly to and promotes Tas for ubiquitination and degradation. And the RBCC domain of Trim28 is required for the ubiquitination and degradation of Tas. Conclusions Collectively, our findings not only identify a host factor Trim28 negatively inhibits PFV replication by acting as transcriptional restriction factor enriched in viral LTR promoter through modulating H3K9me3 mark here, but also reveal that Trim28 mediated ubiquitin proteasome degradation of Tas as a mechanism underlying Trim28 restricts Tas-dependent transcription activity of PFV promoter and PFV replication. These findings provide new insights into the process of PFV latency establishment. Graphical Abstract


2008 ◽  
Vol 63 (3-4) ◽  
pp. 277-283 ◽  
Author(s):  
Xu Ai Lin ◽  
Yin Chen ◽  
Wei Hua Xu ◽  
Yong Zhu Yi ◽  
Zhi Fang Zhang

Autographa californica multicapsid nucleopolyhedrovirus (AcMNPV) encodes an ubiquitin protein, which may be involved in virus infection. Functional analysis of the AcMNPV ubiquitin promoter was performed by progressive deletion of sequence or mutation of putative cis-activating motifs in the promoter region. In the presence of viral factors, a transient expression assay demonstrated that the active regions responsive to promoter transcription are mainly located within the range of -595 to -382 bp upstream of ATG. A 196-bp fragment (-383 to -187 bp), consisting of the distal TAAG, CAAT motif and TATA box, could also drive the expression of a reporter gene. Site-directed mutagenesis analyses indicated that mutations of TATA boxes and TAAG motifs reduce the promoter activity remarkably, while CAAT mutations enhance the promoter activity by about 3- or 4-fold as compared to the native promoter. All the results suggested that two continuous promoter regions are involved in the transcription of the ubiquitin gene and the cis-activating motifs corresponding to viral factors are mainly present within the 5′ region of the promoter. In addition, CAAT motifs in the promoter region function as negative regulator(s) binding sites


2000 ◽  
Vol 68 (10) ◽  
pp. 5970-5978 ◽  
Author(s):  
Sandra I. Resto-Ruiz ◽  
Debra Sweger ◽  
Raymond H. Widen ◽  
Nikola Valkov ◽  
Burt E. Anderson

ABSTRACT Bacterial htrA genes are typically activated as part of the periplasmic stress response and are dependent on the extracytoplasmic sigma factor rpoE. A putative promoter region, P1, of the ςE-type heat-inducible promoters has previously been identified upstream of the htrA gene ofBartonella henselae. Further analysis of thehtrA mRNA by primer extension demonstrated that transcription initiates from P1 and a second region downstream of P1. This second promoter region, termed P2, had no sequence identity to ςE-type heat-inducible promoters. Promoter regions were cloned individually and in tandem into pANT3 upstream of a promoterless version of the green fluorescent protein (GFP) gene (gfpmut3) and transformed into B. henselae by electroporation. The contiguous promoter region containing both P1 and P2 were necessary for the optimal transcriptional activation of thehtrA gene. Promoter activity at 37°C was distinctively higher than at 27°C. However, thermal induction at 47°C did not increase expression of gfpmut3. Invasion of human microvascular endothelial cells (HMEC-1) by B. henselaeresulted in the formation of well-defined vacuoles containing clusters of bacteria exhibiting marked expression of gfpmut3transcribed from the P1-P2 region. In addition, a moderate yet significant increase in the ratio of bacterial GFP to DNA was detected for intracellular bacteria compared to extracellular bacteria, indicating upregulation of htrA upon invasion of HMEC-1. The activation of specific genes in the intracellular environment may help us better understand the novel pathogenic mechanisms used by this bacterium.


2008 ◽  
Vol 31 (4) ◽  
pp. 11
Author(s):  
Manda Ghahremani ◽  
Courtney W Hannah ◽  
Maria Peneherrera ◽  
Karla L Bretherick ◽  
Margo R Fluker ◽  
...  

Background/Purpose: Premature ovarian failure (POF) affects 1% of women with a largely idiopathic and poorly understood etiology. The objective of this study was to identify specific epigenetic alterations by measuring DNA methylation of gene regulatory regions in women with POF vs. controls. Methods: Blood samples were collected from idiopathic POFpatients (Amenorrhea for at least 3 months and 2 serum FSH levels of > 40mIU/ml obtained > 1 month apart prior to age 40) and control women (CW) (healthy pregnancy after age 37 with out a pregnancy loss). Genomic DNA was extracted from EDTA anticoagulated blood and bisulfite converted for analysis using the Illumina Golden Gate Methylation Panel which measures DNA methylation at 1506 CpG sites in the promoter regions of 807 genes in 10 POF and 12 CW. Candidate genes with altered epigenetic marks between POF and CW at a nominal P-value < 0.05 were identified using a t-testcomparison within the Illumina bead studio software. Genes of interest were further analyzed for quantitative methylation at specific CpG sites using pyrosequencing in 30 POF and 30 CW. Results: Comparison of DNA methylation profiles of our initial POF and CW groups identified several genes with statistically significanthyper- or hypo- methylation in the POF group (P < 0.05), including the Androgen Receptor (AR)promoter region, which was significantly hypermethylated. To further validate these results, DNA methylation of the AR gene promoter was quantified bypryosequencing in a larger group of POF and CW. Pyrosequencing further confirmed a significantly higher DNA methylation of the AR promoter region inPOF vs. CW (P=0.007). Conclusions: This is a novel study identifying epigenetic alterations in POF. The hypermethylation of the AR gene in POF patients may cause decreased level of the AR in these women. This is especially interesting given a recent report of induced POF in AR deficient mice^1. Specific epigenetic markers, as identified by DNA methylation array profiling in blood, may serve as useful biomarkers for POF and other fertility disorders. However, it will need to be determined if these methylation changes are present prior to diagnosis, or are a consequence of menopause itself. Reference: 1.Hiroko S. et al. Premature ovarian failure in androgenreceptor deficient mice. PNAS;103:224-9


1992 ◽  
Vol 267 (36) ◽  
pp. 26011-26016 ◽  
Author(s):  
Y.S. Li ◽  
R.M. Hoffman ◽  
M.M. Le Beau ◽  
R Espinosa ◽  
N.A. Jenkins ◽  
...  

2000 ◽  
Vol 74 (5) ◽  
pp. 2084-2093 ◽  
Author(s):  
Joel Schaley ◽  
Robert J. O'Connor ◽  
Laura J. Taylor ◽  
Dafna Bar-Sagi ◽  
Patrick Hearing

ABSTRACT The adenovirus type 5 (Ad5) E4-6/7 protein interacts directly with different members of the E2F family and mediates the cooperative and stable binding of E2F to a unique pair of binding sites in the Ad5 E2a promoter region. This induction of E2F DNA binding activity strongly correlates with increased E2a transcription when analyzed using virus infection and transient expression assays. Here we show that while different adenovirus isolates express an E4-6/7 protein that is capable of induction of E2F dimerization and stable DNA binding to the Ad5 E2a promoter region, not all of these viruses carry the inverted E2F binding site targets in their E2a promoter regions. The Ad12 and Ad40 E2a promoter regions bind E2F via a single binding site. However, these promoters bind adenovirus-induced (dimerized) E2F very weakly. The Ad3 E2a promoter region binds E2F very poorly, even via a single binding site. A possible explanation of these results is that the Ad E4-6/7 protein evolved to induce cellular gene expression. Consistent with this notion, we show that infection with different adenovirus isolates induces the binding of E2F to an inverted configuration of binding sites present in the cellular E2F-1 promoter. Transient expression of the E4-6/7 protein alone in uninfected cells is sufficient to induce transactivation of the E2F-1 promoter linked to chloramphenicol acetyltransferase or green fluorescent protein reporter genes. Further, expression of the E4-6/7 protein in the context of adenovirus infection induces E2F-1 protein accumulation. Thus, the induction of E2F binding to the E2F-1 promoter by the E4-6/7 protein observed in vitro correlates with transactivation of E2F-1 promoter activity in vivo. These results suggest that adenovirus has evolved two distinct mechanisms to induce the expression of the E2F-1 gene. The E1A proteins displace repressors of E2F activity (the Rb family members) and thus relieve E2F-1 promoter repression; the E4-6/7 protein complements this function by stably recruiting active E2F to the E2F-1 promoter to transactivate expression.


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